Akita H, Yokoyama M
First Department of Internal Medicine, School of Medicine, Kobe University.
Nihon Rinsho. 1998 Oct;56(10):2471-6.
Acute coronary syndrome is caused by disruption of a coronary atherosclerotic plaque. It is recognized that the risk of plaque disruption depends more on plaque composition than on plaque size. Therefore, it is important to establish imaging techniques and clinical markers for the identification of vulnerable plaques. Intravascular ultrasound and angioscope may reveal important features of vulnerable plaques. In the near future, optical coherence tomography and intravascular thermography may further improve the characterization of plaques. Systemic markers of inflammation, such as CRP and SAA, may reflect the intensity of inflammation in the atherosclerotic lesion. Clinical observations indicate that plaques may be stabilized by lipid-lowering drugs, anti-oxidants, estrogen and Chlamydia-killing antibiotics. After plaque rupture, new generation antiplatelet and anticoagulant drugs, such as GPIIb/IIIa antagonists and low-molecular heparin, can limit the mural thrombi formation more effectively.
急性冠状动脉综合征是由冠状动脉粥样硬化斑块破裂所致。人们认识到,斑块破裂的风险更多取决于斑块成分而非斑块大小。因此,建立用于识别易损斑块的成像技术和临床标志物很重要。血管内超声和血管镜可能揭示易损斑块的重要特征。在不久的将来,光学相干断层扫描和血管内热成像可能会进一步改善对斑块的特征描述。炎症的全身标志物,如CRP和SAA,可能反映动脉粥样硬化病变中的炎症强度。临床观察表明,降脂药物、抗氧化剂、雌激素和抗衣原体抗生素可能使斑块稳定。斑块破裂后,新一代抗血小板和抗凝药物,如GPIIb/IIIa拮抗剂和低分子肝素,能更有效地限制壁血栓形成。